ATRIAL FIIBRILATION  not seen; there’s no p wave that can be

appreciated due to very chaotic atrial activity

Atrial Fibrillation is characterized by a total
 Fibrillatory (f) waves
disorganization of atrial electrical activity due to
multiple ectopic foci resulting in loss of effective atrial
contraction. The dysrhythmia may be chronic or
intermittent.

Types:

1. Paroxysmal (occurs in episodes within <7 days) Figure 1Note: this strip is from lead V1
2. Persistent (occurs in >7 days, requires >less distinctive than atrial flutter (w/c has sawtooth like
cardioversion) wave)
3. Permanent (persistent a-fib, treatment is no >impulses have chaotic random pathways in atria that
longer focused in controlling heart rhythm, cause this tracing
instead in patient’s comfort only)

Atrial Fibrillation may be transient, starting and PR interval

stopping suddenly, and occurring for a very short  not measurable
time (paroxysmal), or it may be persistent, QRS complex
requiring treatment to terminate the rhythm or to  usually normal but may be abnormal
control ventricular rate.
>atrial and ventricular rates are different
Clinical Associations >if ventricles don’t receive impulses from SA node,
Atrial fibrillation usually occurs in the patient with an there would be either fast or slow ventricular contraction
underlying heart disease (e.g. CAD, Rheumatic heart
disease, cardiomyopathy, heart failure). Clinical Significance
 Decrease of carbon dioxide because of
CAUSES ineffective atrial contractions or loss of atrial
- Thyrotoxicosis (thyroid storm) kick, and/or rapid ventricular response.
- alcohol intoxication (holiday heart syndrome in  Thrombi may form in the atria as a result of
western countries) blood stasis.
o alcohol contributes to obesity, HPN, sleep  Pts. w/ a-fib have significant increase risk for
disordered breathing stroke 7 times as compared to general
- caffeine use (not directly causes a-fib) population
- electrolyte disturbances o Embolized clot may develop and pass to
- stress the brain causing stroke. The overall risk
- cardiac surgery increases fivefold with atrial fibrillation.
Risk of stroke is even higher in patients
ECG Characteristics with structural heart disease, with
Rate & Rhythm hypertension, and over 65 years old.
o CHADSVAS – a tool to determine
 Atrial: 350 – 600bpm (irregular) patient’s risk for stroke
 Ventricular: 50-180bpm (irregular)  A-fib can be asymptomatic w/c may indicate a
more serious cardiac problem; not a life-
*If ventricular rate is < 100, it is termed as AFib with
threatening in general BUT if tumagal (sustain
slow or controlled ventricular response; if > 100bpm,
a-fib), could be dangerous.
it is described as AFib with rapid ventricular response.

P wave SIGNS & SYMPTOMS

- Palpitations
 - Chest pain (angina) – because faster heartbeats o Instead the doctor will just give long-
put your heart under strain without pumping off term anti-coagulation therapy – required
enough blood supply if drugs or cardioversion did not convert
- Fainting atrial fibrillation to normal sinus
- Cardiomyopathy (CHF w/c includes shortness of rhythm. Warfarin is the drug of choice,
breath and edema) and patient is monitored for therapeutic
TREATMENT levels.
Goal of treatment: >2 types of cardioversion
- depends on its cause & duration, the patients, a. electrical cardioversion (electric shock)
symptoms, age, and comorbidities b. chemical cardioversion (drugs)
- prevention of cerebral embolic events
Radiofrequency catheter ablation & Maze procedure
Medications:
 For controlling the rate:  For patients with drug-refractory AFib, or who
o Ca channel blockers (e.g. verapamil, cannot or who choose not to have long term
anticoagulation therapy
diltiazem)
o Beta-adrenergic blockers
a. Radiofrequency Catheter Ablation – is a
o Digoxin (cardiac glycoside) – has a very procedure done by guiding a wire into your heart
narrow therapeutic index and destroys small areas of tissue that may be
causing abnormal heartbeats with the use of low
>MAIN GOAL for atrial flutter and a-fib: radiofrequency
 prevent circulatory instability by controlling the b. Maze procedure – it is a surgical intervention
rate and rhythm that stops atrial fibrillation by interrupting the
 prevent coagulations of the blood ectopic electrical signals that are responsible for
the dysrhythmia.
 prevent circulatory stroke
Incisions are made in both atria to stop the
formation and conduction of these signals. The
>Cardioversion
scar tissue generated will permanently block the
 immediate indication if patient is cardiovascular path of ectopic signals that cause atrial
unstable due to uncontrolled tachycardia fibrillation and restores normal sinus rhythm.
 medical procedure done to correct abnormal The use of cold (cryoablation) or heat (high-
heartbeats and restore a normal sinus rhythm; it intensity ultrasound) are the two modifications
is done by sending electric shocks through the of Maze procedure.
electrodes placed on the chest
For prevention of recurrence and maintenance of sinus
 For patients who have been in atrial fibrillation rhythm, drugs may be prescribed:
for more than 48 hours, anticoagulation
therapy with warfarin is recommended for 3-4 - Disopyramide
weeks prior to cardioversion attempt and 4-6 - Flecainide
weeks after successful cardioversion. - Propafenone
o Meaning if pt. has a-fib for more than 48 - Sotalol
hrs, don’t give him cardioversion right - Amiodarone
away bc. it may dislodge the clot formed
in heart to the brain >In controlling the rate, we don’t convert the
 Prior to the procedure, a transesophageal rhythm; because the rhythm control is done via
echocardiogram may be performed to rule out cardioversion with drug maintenance
presence of thrombi or clots in the atria. The
>In rate control, beta-blockers, preferably cardio-
cardioversion procedure can cause the clots to
selective beta-blockers, are used (e.g. propranolol,
dislodge, placing the patient at risk for stroke. If
bisoprolol, atenolol)
clots are seen, then, the procedure is
contraindicated.
>Amiodarone – has some AV nodal effect; via IV; can
be used if other agents are contraindicated or ineffective;
can also be used for hypotensive pts.
>Diltiazem – is more effective than Digoxin
>Anticoagulant for a-fib and atrial flutter – aspirin
- however, there is now limited use of aspirin due
to its adverse effects in the long run
- instead, we give heparin & warfarin
(simultaneously)
- heparin administration is stopped at the 5th
day but warfarin will still continue to be
given; because warfarin needs to reach its serum
level before its therapeutic effect to occur

Pacemaker implantation or surgery is required for

patients who are unresponsive to medications.

To prevent postoperative atrial fibrillation:

 preoperative administration of beta blocker ATRIOVENTRICULAR JUNCTIONAL
 immediate postoperative administration of IV DYSRHYTHMIA
amiodarone - If the SA node fails to fire and the impulse is not
 prophylactic atrial pacing initiated in other ectopic sites in the atria, the
AV junction is the next pacemaker for the heart.
- The AV junction includes the AV node and the
bundle of His, which branches into the right and
left bundle branches.

Junctional Dysrhythmias

 Refer to as the cardiac rhythms that are

generated from the area around the AV junction
node
 An impulse arising from the AV junction may
occur in response to failure of higher
pacemakers, or it may result from an abnormal
mechanism, such as altered automaticity.
2 major types of dysrhythmias that arise in AV
junction:
a. Disturbances in automaticity, with the AV
junctional tissue assuming the role of the
pacemaker
b. Disturbances in conduction, with the AV
junction blocking impulses journeying from
atria to the ventricles
Inherent Heart Rates
- SA node = 60-100 bpm
- AV node = 40-60 bpm
- Bundle of His = 40-60 bpm
 - L & R bundle branches = 20-40 bpm  anxiety from daily emotional struggle
- Purkinje fibers = 20-40 bpm & diseases can contribute to stress and
inflammation to the heart
>Junctional dysrhythmia may serve as a warning of a
 If PJC occurs occasionally, then the
more serious dysrhythmia
cause is insignificant.
>Junctional rhythm not caused by complete heart block  If it occurs frequently, then
has the following characteristics: tachycardia of junctional ectopics may
be the reason. Because beat generate
>Junctional rhythm is not dependable as the long-term
earlier than usual before arrival of
cardiac pacemaker because its intrinsic rate is slow and
sinus impulse.
more irritable ectopic foci may fire, such as from the
- Pathophysiology
ventricles.
Premature Junctional Complex
Disturbances in Automaticity
- PJC is an impulse that starts in the AV nodal
1. Premature Junctional Comples/Contraction (PJC)
area before the next normal sinus impulse
- A premature junctional complex is a contraction
reaches the AV node
that occurs early and before the next normal
sinus impulse.
- PJCs originates in the AV junction and
prematurely occurs before the next expected P-
wave.
- Isolated PJCs may occur in healthy people and
are insignificant.
- Less common than PAC
- Causes:
o Idiopathic but it is due to abnormality in
depolarization that arises from His
purkinje system
o PJCs may be found in healthy individuals,
or they may be the result of excessive
intake of: - Assessment
 Stimulants Clinical Manifestations
 Caffeine, tobacco, alcohol
 Digitalis toxicity- overdose of digoxin  Usually clients can tolerate junctional rhythms
can cause over contractility of the heart, without significant loss of cardiac output;
can lead to heart failure however, clients with underlying diseases may
o Diseases become symptomatic depending upon the
 Hyperthyroidism - due to the increase amount and frequency of ectopic beats.
production of the thyroid hormone o Anxiety
which forces the heart to work harder o Palpitations
than usual; therefore, increasing the o Shortness of breath
metabolism, HR and BP  Clients are usually asymptomatic, and no
 Coronary Artery Disease, Heart interventions are warranted
Failure, Inferior MI, Hypoxia,  Obtain a complete history of all illnesses, dietary
COPD – because it contributes stress restrictions, and activity restrictions and a
to the heart. (e.g. coronary artery current medication history.
disease—narrowing of the blood
vessels thereby forcing more work to - Diagnostics and Laboratories
the heart)
Electrocardiogram (ECG)
o Stress
  detects specific conduction defects and monitors o inotropic drug-increases
the patient’s cardiac response to electrolyte contractility of the heart, could be
imbalances, drug effects, and toxicities the reason that the heart is
 Characteristics: prematurely contracting
o Rhythm: Regular or Irregular; Early beat  Antidysrhythmic can also be given (e.g.,
disrupts rhythm Quinidine sulfate, phenytoin) to suppress
o P wave: inverted or absent, may follow the frequent PJCs
QRS, or may occur before the QRS
>Junctional dysrhythmias are commonly iatrogenic in
o because the impulse moves from the AV
nature secondary to medication intake such as digoxin; if
node up to the atria instead of from the SA it is drug-induced, terminate the immediately
node down toward the AV node.
o PR interval: PR interval shortens to less >Digoxin has very narrow therapeutic index so it needs
than 0.12 seconds close monitoring; esp those who undergo drug
o QRS: Usually normal, consistent in shape maintenance with digitalis – the nurse needs to know the
(0.06-0.10 seconds) schedule of laboratory tests to see if they already
 Conduction reached the toxicity levels
o Irritable site in AV junction fires before - Additionally, digoxin is very high-protein bound
next SA node impulse is due so they can accumulate in the body easily and
o Impulse is conducted normally through reach toxicity
ventricles
o Compensatory pause often follows a PJC SUPRAVENTRICULAR TACHYCARDIA
Supraventricular tachycardia (SVT), also called
paroxysmal supraventricular tachycardia, is defined
as an abnormally fast heartbeat. It's a broad term that
includes many forms of heart rhythm problems (heart
arrhythmias) that originate above the ventricles
(supraventricular) in the atria or AV node.
JUNCTIONAL TACHYCARDIA
- a form of supraventricular tachycardia, a type of
racing pulse caused by a problem in the area between the
upper and lower chambers of your heart. It’s known as
the atrioventricular node, or AV node.
>The main difference of PJC to PAC is the P wave (w/c
could either be absent or inverted) and the PR interval >here the AV node takes over the SA node as the
pacemaker of the heart
- Treatment:
- When it occurs in adults and elderly, it is
Pharmacological and Medical Care
referred to as non-paroxysmal junctional tachycardia
a. Non-pharmacologic (NPJT) whereas it is referred to as junctional ectopic
 Treatment is usually not required for tachycardia (JET) in children
infrequent PCJs
Signs and Symptoms
 Encouraged lifestyle changes (reduce
caffeine intake, exercise, stop smoking and - A racing or fluttering heart
alcohol intake) - Shortness of breath
b. Pharmacologic - Sweating
 If PCJs are frequent, treat the underlying - Headache
cause first - Dizziness or lightheadedness
 If digitalis toxicity is the cause, discontinue - Fainting
or adjust the dosage of digoxin NON-PAROXYSMAL JUNCTIONAL
TACHYCARDIA
  also called Accelerated AV junctional rhythm Pathophysiology
 occurs when the rate of an AV junctional
pacemaker exceeds that of the sinus node. This
situation arises when there is increased
automaticity in the AV node coupled with
decreased automaticity in the sinus node.
 Not a common occurrence; usually only happens
due to digitalis toxicity
Digoxin also has direct effects on conduction through
Characteristics increased vagal tone. Digoxin stimulates the vagus nerve
leading to prolonged conduction through the sinuatrial
- The rate of junctional discharge is only moderately (SA) and atrioventricular (AV) nodes. Overall, digoxin
increased, being about 70 to 130 beats/min. slows the conduction and increases the refractory period
- NPJT appears to reflect an increase in A-V junctional in cardiac tissue by enhancing vagal tone.
automaticity, which allows the A-V junction to become >Digoxin toxicity
the dominant pacemaker controlling the ventricles.
 doesn’t cause only 1 type of dysrhythmia
Causes – idiopathic in nature pa rin; associations lang
 very fatal (it can cause cardiac arrest)
ang following
Medical Interventions
- Digoxin toxicity (= the classic cause of AJR)
- Beta-agonists, e.g. isoprenaline, adrenaline  Since NPJT is usually secondary to either
- Myocardial ischemia digitalis intoxication or myocardial infarction,
- Myocarditis therapy should be directed toward the primary
- Cardiac surgery problem.
o In the former case, digitalis should be
Diagnosis and Laboratory
discontinued, since NPJT may be a
 The diagnosis of NPJT depends upon the forerunner of a more serious arrhythmia.
demonstration of a gradual acceleration of the Potassium can be administered if the
junctional pacemaker. The junctional beats may patient is hypokalemic.
have associated retrograde P waves. More  In acute myocardial infarction, the arrhythmia is
frequently, the diagnosis of NPJT is made in the generally self-limited and does not necessitate
presence of A-V dissociation. therapy.
 If loss of atrial transport function is
 The doctor will ask about your health history hemodynamically troublesome, administration
and symptoms. They will do an of atropine may restore sinus rhythm by
electrocardiogram to look at the electrical increasing sinus rate and facilitating A-V
pulsing of your heart. They will also look for conduction. 
signs that your AV node has taken over the
>Additional: Monitor serum electrolytes
rhythm-setting job of the heart.
ATRIOVENTRICULAR NODAL REENTRY
TACHYCARDIA (AVNRT)
» can be also called:
- Junctional reciprocating tachycardia
 This rapid ECG rhythm includes narrow QRS - Reciprocal or reciprocating AV nodal reentrant
complexes, an absence of P waves prior to each tachycardia
QRS and a rate faster than 100 bpm. - AV junctional reentrant tachycardia
 Notice the inverted waveform after many of the
QRS complexes, which is a possible further
evidence for junctional tachycardia
● most common type of super ventricular
tachycardia
● responsible for 50-60% of tachycardias narrow – less filling of the ventricles leads to
QRS in adults and 15% of supraventricular tachycardias the reduction in cardiac output and the decreased
in pediatric patients, predominantly from adolescence perfusion of the brain
onwards
- cardiac arrest - 2.2% to 4.5% of patients with
● episodes often start and end suddenly, and occur accessory pathways
because of a reentrant circuit — also called an accessory - patients with avnrt and known coronary artery
pathway — located in or near the AV node that causes disease may present with myocardial infarction
the heart to beat prematurely – may also complain chest pain
– may have symptoms of heart failure
● tends to occur more often in young women, but
achypnea with wheezes or swelling in the lower
it can affect both males and females of any age
extremities on physical exam
● there is a female predominance, with a ratio of -
2:1 or 3:1. Its manifestation occurs mainly during the
Pathophysiology
third or fourth decade of life.
AVNRT is caused by a reentry circuit in or around the
● tachycardia typically ranges between 140-280
AV node.
bpm and is regular in nature
Occurs when an impulse is conducted to an area in the
● Ventricular and atrial rhythm: Regular;
AV Node that causes the same impulse to be rerouted
sudden onset and termination of the tachycardia
back into the same area over and over again at a very
● it may cease spontaneously (and abruptly) or fast rate. Each time the impulse is conducted through
continue indefinitely until medical treatment is sought this area it is also conducted down into the ventricles
causing a fast ventricular rate
Causes
The circuit is formed by the creation of two pathways
- Nicotine forming the re-entrant circuit, namely the slow and fast
- Coffee pathways.
- Alcohol
- Stimulants The fast pathway is usually anteriorly situated along
- Exercise septal portion of tricuspid annulus with the slow
- Surges in vagal tone pathway situated posteriorly, close to the coronary sinus
ostium.
Precipitating factors
Sustained reentry occurs over a circuit comprising the
- physical activities AV node, His Bundle, ventricle, accessory pathway and
- Sudden movement atrium.
- Emotional stress
The various forms of AVNRT can be described in terms
Clinical manifestations of ECG appearance such as R-P intervals or Slow/Fast
- Intermittent palpitations pathway dominance.
- Fatigue
- Chest pain
- Light headedness
- Neck discomfort (be careful in assessing the
carotid)
- Frog sign
- Polyuria
- Pre-syncope
- syncope – can occur between 15% and 20% of
patients, due to the high rate of the
tachyarrhythmia (≥ 170 bpm)
Sample ECG tracing:
 o In most cases this results in a ‘typical’
SVT appearance with absent P waves and
tachycardia
Fast-slow

 Accounts for 10% of AVNRT

 Associated with Fast AV nodal pathway for
anterograde conduction and Slow AV nodal
pathway for retrograde conduction.
 The retrograde P wave appears after the
corresponding QRS
 ECG
o QRS -P-T complexes
Characteristics o P waves are visible between the QRS
● Atrial rate – usually 150 to 250bpm and T wave

● Ventricular rate usually 120-200bpm

● QRS shape and duration: Usually normal but
may be abnormal
● P wave: Usually very difficult to discern
● PR interval: If the P wave is in front of the QRS,
the PR interval is less than 0.12 seconds

Classification: Slow-fast and Fast-slow

Slow-fast Diagnostics and Laboratories

 Accounts for 80-90% of AVNRT - Blood tests (to see if the pt. is anemic)
 Associated with Slow AV nodal pathway for - Pregnancy test
anterograde conduction and Fast AV nodal - ECG
pathway for retrograde conduction. - Holter monitor
 The retrograde P wave is obscured in the - Echocardiogram (structural)
corresponding QRS or occurs at the end of the - Stress test (tolerance activities; how your heart
QRS complex as pseudo r’ or S waves works under stress, e.g manipulating the speed
 ECG: of treadmill)
o P waves are often hidden – being - Electrophysiological testing and mapping
(tinitingnan kung san may problem at kung saan
embedded in the QRS complexes.
nagaganap yung reentry excitations)
o Pseudo r’ wave may be seen in V1
o Pseudo S waves may be seen in leads II, III Pharmacology and Medical care
or aVF.
 Vagal maneuver – you may be able to stop an
episode of AVNRT by using particular
maneuvers that include holding your breath and
straining, dunking your face in ice water, or
coughing
 Carotid massage – you may be able to stop an
episode of AVNRT by using particular
maneuvers that include holding your breath and
straining, dunking your face in ice water, or
coughing
  Ice and cold wet towel
 Valsalva maneuver – to increase intrathoracic
pressure of 40 mmHg for 15 seconds, by
expiring against a closed glottis
 Cardioversion – if you're unable to stop an
episode on your own using vagal maneuvers,
your doctor may use cardioversion, which can
be conducted as a procedure or by using
medications
o Cardioversion is rarely used on patients
with AVNRT, usually when the
tachycardia is refractory to other
medical therapies or the tachycardia is
causing haemodynamic instability
(falling blood pressure, development of
heart failure etc.)
o Cardioversion is usually done with
electric shocks, which are given through
electrodes attached to your chest while
you're sedated

Nursing Considerations (in general, for

Supraventricular Tachycardia)
- Continuously monitor ECG for rate, rhythm, and
conduction. Assess vital signs and associated symptoms
with changes in ECG. Report findings to physician.
- Explain the importance of rapidly reducing the
heart rate.
- Encourage verbalization of fears and concerns.
Answer questions honestly, correcting misconceptions
about the disease process, treatment, or prognosis.
- Explain to the client possible treatments or
medications to be considered; must adhere to the
doctor’s instructions when medications are given